Disease progression models

Amyotropic lateral sclerosis (ALS) 3. AEA and 2-AG increase in the spinal cord of SOD1 transgenic mice, a model of ALS, to inhibit disease progress 3. CB2 receptor agonists or inhibitors of degradation... 

Similarly, under certain disease conditions, altered NA innervation and/or AR signaling capacity impairs sympathetic communication with cells of the immune system, influencing disease progression. Altered catecholamine communication with the immune system is evident in autoimmune diseases such as arthritis and multiple sclerosis [5-7] and in infectious diseases, such as leprosy and a mouse model of acquired immunodeficiency syndrome [15, 43, 44], The impact of altered NA innervation of... 

Sugai F, Yamamoto Y, Miyaguchi K, Zhou Z, Sumi H, Hamasaki T, Goto M, Sakoda S (2004) Benefit of valproic acid in suppressing disease progression of ALS model mice. Eur J Neurosci 20(11) 3179-3183... 

In the third example, DIMS9054 but not DIMS9052 was able to reduce the rate of disease progression in the EAE in vivo rat model (Fig. 4) despite the fact that both DIMS have similar primary structures (see Notes 7, 13). 

In projecting results of short-term trials over patients lifetimes, it is typical to present at least two of the many potential projections of lifetime treatment benefit. A one-time effect model assumes that the clinical benefit observed in the trial is the only clinical benefit received by patients. Under this model, after the trial has ended, the conditional probability of disease progression for patients is the same in both arms of the trial. Given that it is unlikely that a therapy will lose all benefits as soon as one stops measuring them, this projection method generally is pessimistic compared to the actual outcome. A continuous-benefit effect model assumes that the clinical benefit observed in the trial is continued throughout the patients lifetimes. Under this model, the conditional probability of disease progression for treatment and control patients continues at the same rate as that measured in the clinical trial. In contrast to the one-time model, this projection of treatment benefit most likely is optimistic compared to the treatment outcome. 

Tortarolo M., Veglianese P., Calvaresi N., Botturi A., Rossi C., Giorgini A., Migheli A., and Bendotti C. (2003). Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression. Mol. Cell. Neurosci. 23 180-192. 

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